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  Table of Contents     
Year : 2011  |  Volume : 57  |  Issue : 2  |  Page : 138-140

Fresh look at the doppler changes in pregnancies with placental-based complications

Department of Radiology, Nowrosjee Wadia Hospital, Parel, Mumbai, India

Date of Web Publication4-Jun-2011

Correspondence Address:
S Dikshit
Department of Radiology, Nowrosjee Wadia Hospital, Parel, Mumbai
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0022-3859.81880

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 :: Abstract 

Placental-based complications of pregnancy can be classified as acute and chronic. An example of acute placental complication is abruptio placenta. The chronic placental complications include pregnancy induced hypertension (PIH) and idiopathic Intrauterine growth restriction (IUGR). The fetus is at risk for perinatal complications in both acute and chronic conditions. Here we take a look at the natural history of the Doppler parameters in chronic conditions. The techniques used for assessing the fetal well-being include, clinical methods, biophysical tests, conventional ultrasonography, and fetal Doppler studies. Arterial Doppler studies are used to assess the well-being of the fetus and to determine the timing of delivery. However, arterial Dopplers predict only the subset of fetuses at risk of having perinatal complications. Venous Dopplers have been used to improve upon the prognostication. However, by the time the commonly used venous Doppler signs, that is, 'A' wave reversal in ductus venosus (DV) is present, the fetus is likely to be already compromised. The fetus tries to adapt to the environment of deprivation by making a series of changes in the umbilical artery circulation, cerebral circulation, and hepatic circulation. As a result of these adaptations, the fetus overcomes the state of chronic hypoxia. This article takes a look at these changes and also the effect of these adaptations. It is suggested that serial comparisons of the venous flow characteristics of the DV and inferior vena cava (IVC) can provide an early indication of the impending decompensation and can be used to predict the time the delivery.

Keywords: Arterial Dopplers, Doppler, ductus venosus, IUGR, IVC, PIH, placental-based pregnancy complications, venous Dopplers

How to cite this article:
Dikshit S. Fresh look at the doppler changes in pregnancies with placental-based complications. J Postgrad Med 2011;57:138-40

How to cite this URL:
Dikshit S. Fresh look at the doppler changes in pregnancies with placental-based complications. J Postgrad Med [serial online] 2011 [cited 2023 Sep 30];57:138-40. Available from:

The placental-based complications of pregnancy can be classified as being acute and chronic in etiology. An example of the acute placental complication is abruptio placenta. Chronic placental complications include pregnancy induced hypertension (PIH) and idiopathic intrauterine growth restriction (IUGR). The fetus is at risk for perinatal complications in both acute and chronic conditions. Here we take a look at the Doppler ultrasound analysis for assessing the fetal well-being in chronic conditions. The various techniques used for assessing the fetal well-being include the clinical method (kick count), Biophysical tests (non-stress test, contraction stress test, Fetal Biophysical Profile), routine sonographic assessment (fetal growth, liquor), and Doppler studies. The Doppler studies look at the arteries,such as the umbilical artery, middle cerebral artery, and descending thoracic aorta, or veins like DV, IVC, and the umbilical vein. The challenge in the treatment of a gravida with a chronic placental condition like PIH or IUGR lies in deciding when to deliver the baby. Aggressive management in the form of early delivery is fraught with dangers of perinatal morbidity and mortality, due to iatrogenic prematurity; and procrastination of delivery is fraught with the risk of intrauterine fetal death or fetal brain damage. Doppler assessment is used in these cases, as it allows for serial and progressive assessment of the condition. [1] The delivery can then be timed optimally.

It is generally accepted that arterial Doppler changes precede venous Doppler changes. [1] However, it has recently been documented that there are situations where the arterial indices do not warrant early delivery, but a simultaneous assessment of the venous indices show that they are abnormal. [2] This article takes a look at the changes that happen in these conditions in the maternal and fetal circulation. Knowledge of these changes can help a clinician in managing the pregnancy better and also in understanding the underlying pathophysiology.

The primary pathology in these conditions is abnormal vascularization of the spiral arterioles feeding the placenta. Normally, there is conversion of these vessels from high resistance vessels to low resistance vessels, by the invasion of the tunica media of the blood vessels by the trophoplastic tissue. Failure of this to happen results in the abnormal conditions mentioned earlier. [3] Baschat, [4] in an editorial, has traced the vascular changes in placental-based conditions. The placental conditions, both acute and chronic, act by the principle of demand and supply. The supply side is represented by the PO 2 in the placental villi and the demand side is determined by the fetal oxygen requirements. When there is a severe mismatch as in abruption placenta or severe PIH, the result is fetal demise. However, when the mismatch is moderate, the fetus makes a series of adaptations, which may tide over the situation on a short-term time frame, but may come at the cost of long time dysfunction. [4] In a study of the fetal heart and the two ventricular outputs using 2D fetal echocardiography, [5] it has been shown that the effect of the placental-based conditions is an increase in the right ventricular after-load, due to increased umbilical artery resistance and a decrease in the left ventricular after-load, due to decreased cerebral resistance. This results in the preferential shunting of blood from the right ventricle (RV) to the left ventricle (LV) via a reversal of the flow in the aortic isthmus. [5] This further leads to dilution of the oxygen-rich blood from the LV going to the cerebral vessels, by blood, poor in oxygen, coming from the RV. This can potentially further reduce the PO 2 in the blood reaching the fetal brain, causing damage. In addition to these changes, the fetus increases the delivery of oxygen-rich blood to the fetal brain by another method. This is achieved by increasing the proportion of umbilical venous flow through the ductus venosus [6] at the cost of the hepatic flow. As a result, the right atrium (RA) receives more oxygen-rich blood from the placenta. It has been shown [7] that at least part of the reason for the increased DV flow is the increased diameter of the vessel. This also contributes to the transmission of the 'A' wave reversal to the umbilical vein in advanced states, in the form of pulsation of the UV. Thus, it is clear that DV adjustments lead to changes in the DV flow, which result in loss of the pressure head. Simultaneously, the changes in IVC, due to an elevated venous return leads to pressure changes in the IVC. [8] These changes are represented in an altered venous velocity index (VVI).

All these changes can be represented in the simplified form as follows

  1. Placental-based pathologies lead to decreased PO 2 in the placental lake.
  2. If the changes are not acute, then the fetus gets time to make adjustments to overcome this condition. The consequences are a result of a mismatch of the demand and supply of oxygen to the fetal tissues.
  3. There are possible ways by which the fetus makes adjustments:
    1. Response of the fetus to hypoxia is to redistribute the blood toward the cerebral circulation. This is achieved by cerebral vasodilatation and is reflected in the decreased middle cerebral artery (MCA) pulsatility index (PI).
    2. Increase in the flow through the cerebral arteries is also facilitated by increased umbilical artery resistance. This leads to a reversal of the flow through the aortic isthmus from the descending aorta toward the ascending aorta.
    3. Increase in umbilical artery resistance is not a selective increase in vascular resistance. It is associated with an increase in the peripheral venous tone. This leads to an altered venous flow pattern in the IVC.
    4. The fetus also increases the proportion of oxygen-rich blood going from the umbilical vein to the RA, by altering the diameter of the DV. This occurs at the cost of blood reaching the portal circulation. Clinically this is expressed in the form of a shrinking fetal liver size, which leads to a decrease in the fetal abdominal circumference (AC).
    5. If the maternal placental changes are not progressive and if the fetus is able to reduce its requirements by compromising its growth (IUGR), then the demand and supply are in equilibrium and the fetus is able to tide over the situation.
    6. However, if there is a mismatch, then the PO2 of the blood being delivered to the fetal tissues, especially the fetal brain starts dropping.
    7. The fetus is on 'Mount Everest' in utero due to peculiarities of the fetal hemoglobin HbF. A minimal drop in the PO2 of the fetal blood results in a massive reduction in the amount of O2 bound to the HbF.
    8. As demand grows more than the supply, the fetus experiences hypoxia. This results in a build-up lactic acid decreased myocardial activity, a reversal of the DV 'A' wave. If unchecked, this can lead to fetal demise.

An important aspect of the fetal vascular adjustments in the initial period is an increase in the venous return to the heart. [5] Although, with increasing venous return the IVC venous flow characteristics change. These can either be a change in the peak systolic velocity or a change in the venous vascular index (VVI). There is simultaneous alteration in the DV flow. This is done to increase the fraction of blood flow from the umbilical vein going to the ductus venosus at the cost of the blood flowing into the portal veins. This change represents changes in the DV peak systolic velocity or changes in the DV venous vascular index. As separation of the IVC flow (carrying blood with relatively low PO 2 ) and DV flow (carrying blood with relatively high PO 2 ) is essential to supply oxygen to the fetal brain, any change in the flow characteristics of the two flows can lead to the premixing of blood. A comparison of the two flows in the form of either ratio of their peak systolic velocities or ratio of the venous vascular indices may identify a trigger point, which tips the fetus from a compensated state to a decompensated state. A multicentric study comparing the flows of DV and IVC, in cases with PIH and IUGR, may be able to tell if these vascular changes precede fetal decompensation.

 :: References Top

1.Turan OM, Turan S, Gungor S, Berg C, Moyano D, Gembruch U, et al. Progression of Doppler abnormalities in intrauterine growth restriction. Ultrasound Obstet Gynecol 2008;32:160-7.  Back to cited text no. 1
2.Baschat AA, Harman CR. Discordance of arterial and venous flow velocity waveforms in severe placenta-based fetal growth restriction. Ultrasound Obstet Gynecol 2011;37:369-70.  Back to cited text no. 2
3.Ochi H, Kusanagi Y, Katayama T, Matsubara K, Ito M. Clinical significance of normalization of uterine artery pulsatility index with maternal heart rate for the evaluation of uterine circulation in pregnancy-induced hypertension. Ultrasound Obstet Gynecol 2003;21:459-63.  Back to cited text no. 3
4.Baschat AA. Integrated fetal testing in growth restriction: Combining multivessel Doppler and biophysical parameters. Ultrasound Obstet Gynecol 2003;21:1-8.  Back to cited text no. 4
5.Tsyvian P, Malkin K, Artemieva O, Blyakhman F, Wladimiroff JW. Cardiac ventricular performance in the appropriate- for-gestational age and small-for-gestational age fetus: Relation to regional cardiac non-uniformity and peripheral resistance. Ultrasound Obstet Gynecol 2002;20:35-41.  Back to cited text no. 5
6.Yagel S, Kivilevitch Z, Cohen SM, Valsky DV, Messing B, Shen O, et al. The fetal venous system, Part II: Ultrasound evaluation of the fetus with congenital venous system malformation or developing circulatory compromise. Ultrasound Obstet Gynecol 2010;36:93-111.  Back to cited text no. 6
7.Kiserud T, Kessler J, Ebbing C, Rasmussen S. Ductus venosus shunting in growth-restricted fetuses and the effect of umbilical circulatory compromise. Ultrasound Obstet Gynecol 2006;28:143-9.  Back to cited text no. 7
8.Fouron JC, Absi F, Skoll A, Proulx F, Gosselin J. Changes in flow velocity patterns of the superior and inferior venae cavae during placental circulatory insufficiency. Ultrasound Obstet Gynecol 2003;21:53-6.  Back to cited text no. 8

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